Infection - Initial, Mechanisms,Variation, Mutations, Evolution - Kolonalisasi infection is performed by a foreign species to the host organism, and are Pilang harm the host. Organism, or pathogen, using facilities owned by the host to be able to reproduce themselves, and ultimately detrimental to the host. Pathogens disrupt the normal function of the host and can result in chronic wounds, gangrene, loss of body organs, and even death. Host response to infection is called inflammation. In general, pathogens are generally categorized as microscopic organisms, although the actual definition is broader, including bacteria, parasites, fungi, viruses, prions, and viroids.
Symbiosis between parasite and host, in which one party gains and one party aggrieved, be classified as parasitism. Branch of medicine that focuses infections and pathogens is infectious disease branch.
In general, infection is divided into two major categories:
Infections that occur due to exposure to the antigen from outside the body
Infections that occur due to diffusion of body fluids or tissues, such as the HIV virus, the virus can not survive outside the body.
Initial infection
After penetrating tissue, the pathogen can be grown outside the body cells (extracellular) or using the body as its host cell (intracellular). Further intracellular pathogens can be further classified:
pathogens proliferate freely in the cell, such as viruses and some bacteria (Chlamydia, Rickettsia, Listeria).
pathogens that multiply in the vesicles, such as mycobacteria.
Penetrated tissue can be damaged due to pathogen infection, such as the exotoxin secreted on the cell surface, or endotoxin that triggers secretion by makrofaga sitokina secretion, and lead to symptoms of local or systemic.
The decline of immune system mechanisms
On a common stage of infection, antigen triggers the immune system will always derivative, and then the artificial immune system during acute. But the path of infection is not always the case, the immune system may fail to extinguish the infection, because there was a focus of infection such as:
subversion of the immune system by pathogens
inherited disorders caused by gene
uncontrolled immune system mechanism
Propagation of pathogenic development depend on the ability of replication in the host and then spreads into a new host by the infection process. To that end, the pathogens are required to proliferate without triggering the immune system, or in other words, the pathogen is required to not undermine its host too quickly.
Pathogens that can survive only pathogens that have developed mechanisms to avoid the triggering of the immune system.
Serotype variationOne way used by pathogens to avoid immune system is to change the structure of the cell surface. Many extracellular pathogens have a very diverse antigenic types. One example is Streptococcus pneumoniae, causing pneumonia, which has many known and new antigenic type 84 range. Each variety has a different structure of the polysaccharide coating. The types are differentiated based on serologic testing, so it is also called serotypes. Infection by one particular serotype may lead to artificial immune system to it, but not against re-infection by different serotypes, because of artificial immune system seen as a single serotype of different types of organisms. Recurrent acute infections of the same antigen can occur because of this.
The use of a protective capsule that prevents lysis by the complement system and phagocytes also performed Mycobacterium tuberculosis. Bacterioides species of commensal bacteria commonly living in the appendix of mammals. Some species such as Bacterioides fragilis is an opportunistic pathogen causing infection of the lining of the peritoneum. This species avoids the immune system by influencing phagocytes perceiving used to ingest bacteria or by masquerading as an organism's cells so the immune system does not recognize them as pathogens.
Bacteria and fungi may also form a complex bio layer, providing protection of cells and proteins of the immune system. Recent research has shown that the bio layer appears in a successful infection, including chronic infection of Pseudomonas aeruginosa and Burkholderia cenocepacia, the main characteristic of cystic fibrosis.
Genetic Mutations
Trypanosome detection by antibodies would trigger a change of VSG genes on the DNA, thus resulting in different VSG proteins. Body will then make a new antibody in the same way, but any newly created antibodies that recognize trypanosome, VSG genes will change again before the immune system is triggered. Thus trypanosome be one step ahead of immune system, so even though the form of a multiply extracellular protozoa, the focus of infection is chronic and form immune complexes and inflammation, until the end of the nerve damage and coma. This causes the disease African trypanosomiasis earned the nickname "sleep". Malaria is another disease caused by protozoan parasites with the ability to re-order DNA, which is very difficult to overcome by the immune system.
The second method is more dynamic demonstrated by influenza virus. Influenza virus is recognized by the immune system via the hemagglutinin found on the surface of the virus.
The first genetic mutation called antigenic drift that changed the notation of the hemagglutinin gene expression, in response to a protein that resides on the surface, neuraminidase. Other mutations that alter epitopes that are not recognized by T cells, especially CD8 has perceiving.
The second genetic mutation called an antigenic shift occurs due to the viral RNA tertukarnya new virus that has long been the host's body.
The third mechanism involves the DNA re-programmed procedures. African trypanosome has the ability to change the major surface antigen multiple times with a single infection. Trypanosome wrapped in a type of glycoprotein called the variant-specific glycoprotein (VSG), which can easily be recognized by the immune system. Nevertheless, trypanosome DNA contains more than 1000 VSG genes with different antigenic expression.
At the level of bacteria, the ability to re-order DNA is also found in Salmonella typhimurium and Neisseria gonorrhoeae.
In physiology, latency is defined as the time interval between stimulus and response is triggered within an organism. Viruses generally soon will coordinate the synthesis of viral proteins needed for proliferation, after the successful conduct of a cell infection. Such mechanisms would result in an acute condition which will be responded by the artificial immune system. T cells can easily scan the fragments of viral proteins are indicated on the surface of MHC molecules and quell the infection.
Nevertheless, there is still another type of virus that can delay the process of viral protein synthesis within the cell. This condition is called latent conditions, when there is no viral replication in cells. Latent infection does not cause disease and the presence of the virus was not detected because there is no viral fragments on MHC molecules. One example is a herpes simplex virus, which did epitelia infection with the focus of the nerve cells in the area.
Once the immune system overcome infection in epitelia, HS virus remains in a latent state in neurons nerve. Several factors such as sunlight, bacterial infections and hormonal changes will activate the virus to migrate through the axon and perform re-infection in epithelial tissues. The focus of infection of neurons has two advantages:
viral peptides produced very little, resulting in fragments that are not flashy
neuron has a class I MHC molecules, which are small, so difficult to detect CD8 T cells.
Another example is the Epstein-Barr virus (EBV), a type of herpes virus to others, has a latent state in B cells Proliferation of B cells will produce new cells with latent EBV infection in dalamnya.Fokus
Evolution of features
Some bacteria are typically ingested by makrofaga with the process of phagocytosis, have evolved and managed to make makrofaga as a focus of infection. One example is Mycobacterium tuberculosis is ingested by makrofaga, will block the disbursement of the lysosome into the phagosome and protect it from sitokina in the lysosomes.
Listeria monocytogenes, can even get out of the phagosome and enter the cytoplasm and to replicate in them. Then infect adjacent cells, without departing from the living intraselularnya.
A protozoan parasite Toxoplasma gondii, can make a vesicle that separates itself from the other cells. This allows T. gondii to create a peptide with the fragments that are not loaded on MHC molecules, so that its presence is not detected the immune system.
Response to pathogens in the face of the immune system is also different. In addition to a variety of ways to escape, some pathogen resistance. Staphylococci aureus releases toxins that two kinds of staphylococcal enterotoxins and toxic shock syndrome toxin-1 which acts as a superantigen.
"Superantigen is a protein that binds to a number of T cell antigen perceiving This bond causes T cell apoptosis is experiencing very fast. "
Other organisms such as Streptococcus pyogenes, and Bacillus anthracis has mechanisms to directly kill phagocytes.
Many pathogens take the fight within the period of acute infection. This is a stress on the immune system (English: immunosuppression) and causes the host's body becomes susceptible to subsequent infection by a pathogen of another kind. Key examples include trauma, burns and major surgery. Patients with burns are not able to respond to infection, so that was a mild infection can cause death.
Measles virus infection is also one example of the pressure on the immune system. Many children suffering from malnutrition are victims, to death, because of subsequent infection when the immune system is suppressed by measles virus infection. Subsequent infection is usually in the form of bacteria that cause pneumonia. Measles virus infection have focused on dendritic cells that affect the performance of T cells and B cells in the immune system, and activation of TH1 cells makrofaga by.
The focus of infection
One of the best examples of this topic is the focus of infection that is owned by the HIV virus, in the form of breaking the chain of cellular immune system because the extinction of the ability of CD4 T cells to become activated and differentiated T helper cells. Chain breaking occurs slowly without sparking the immune system because of the latent nature of retrovirus. A small number of prostitutes Gambia and Kenya are always exposed to HIV infection for 5 years through the reproductive fluid actually showed an immune response and CD8 T cell clone Th1 cells that respond to various HIV epitopes without antibody response.
In addition, the mode used by the HIV virus is a cutting line attached to the information provider with perceiving kemokina CCR5 and CXCR4, in addition to CD4. is an expression of CCR5 perceiving dendritic cells, T cells and CD4 makrofaga. CXCR4 expression was perceiving the CD4 T cells once activated.
Competition in the area perceiving kemokina CCR5 by RANTES secretion, MIP-1α, and MIP-1β showed an immune response against HIV infection.
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